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Hypersensitivity pneumonitis caused by domestic exposure to molds.
14
Citations
4
References
2007
Year
AsthmaMold ControlAdvanced Lung DiseaseLung InflammationAllergenHome EnvironmentLung BiopsyHypersensitivityHypersensitivity PneumonitisPneumothoraxSepsisToxicologyInfection ControlDomestic ExposureAllergyOccupational Lung DiseasesRespiratory DiseasesPulmonary MedicineLung CancerPulmonary DiseasePathogenesisLung MechanicsMedicineEmergency Medicine
Hypersensitivity pneumonitis (HP) is an allergic lung disease related to repeated inhalation of a variety of etiologic agents, many of which have been reported in certain occupations and hobbies, but also in the home environment [2,3]. A 40-year-old woman, a smoker and homemaker, was seen in the emergency room with a history of progressive dyspnea and cough lasting 10 days. The physical examination revealed bilateral crackles. Blood tests showed leukocytosis and hypoxemia. Chest X-ray revealed interstitial infi ltrates. She showed a marked improvement within a few days of hospital admission. After discharge home, she returned to the hospital within 24 hours with a similar clinical picture. High-resolution computed tomography scanning (HRCT) showed bilateral diffuse micronodular infiltrates. Spirometry revealed a forced vital capacity (FVC) 61 % of predicted, a forced expiratory volume in 1 second (FEV 1 ) 42 % of predicted, and a FEV 1 /FVC ratio of 59 %. Lung diffusion capacity (single breath carbon monoxide transfer factor) was 76.2 % of predicted uncorrected but was normal when corrected for alveolar volume. The bronchoalveolar lavage fl uid revealed lymphocytosis with a CD4/CD8 ratio of 1.1. A transbronchial lung biopsy sample showed interstitial pneumonitis and non-necrotizing microgranulomas. Precipitating antibodies to Aspergillus fumigatus were detected in the patient’s serum. She reported that her bathroom was being refurbished because of plumbing problems. A walk-through visit to her house revealed evident water damage and visible mold growing. Cultures of the indoor air obtained by placing agar plates in the house grew mainly A fumigatus and Aspergillus niger. Environmental sampling was performed using a volumetric air sampler and airborne particles were collected onto polytetrafl uoroethylene fi lters [3]. A 39-year-old man, a nonsmoker and waiter, had suffered from dyspnea, cough, fever, and weight loss for the last month. Physical examination revealed bilateral crackles. Blood test showed leukocytosis and hypoxemia. Chest X-ray revealed interstitial infi ltrates. Clinical and radiological signs disappeared within 24 hours. After discharge home, he returned with similar symptoms several hours later. Chest HRCT showed bilateral micronodular infi ltrates and patchy ground-glass opacities. Pulmonary function tests and diffusion capacity were normal. Lymphocytosis and a reduced CD4/CD8 ratio (0.2) in the bronchoalveolar lavage fl uid were observed. Lung biopsy revealed a diffuse interstitial infi ltrate comprised of T-lymphocytes and microgranulomas. Precipitating antibodies to A fumigatus were detected. The patient reported that the rental apartment where he lived had water leakage and dampness. Neither of these subjects kept pets at home or had hobbies or jobs with exposure to suspected antigens. Serologic tests to common respiratory pathogens were negative. Both patients remained symptom free after moving to a different dwelling or remodeling the house. Enzyme-linked immunosorbent assay (ELISA) inhibition studies of immunoglobulin (Ig) G response to A fumigatus showed dose-dependent inhibition with the mold extract and with the extract obtained from the air samples collected at home (fi gure). A diagnosis of HP is made by a combination of clinical, radiological, physiological, and immunological studies. The results of the investigations carried out in our patients indicated that they had developed HP caused by indoor molds (Aspergillus species). Exposure to specifi c domestic indoor fungal spores is considered an unlikely cause of HP [4] except in Japan where summer-type HP caused by home contamination of Trichosporon species is common. In our patients, however, the natural challenge during re-exposure at home, as well as the response to avoidance of exposure strongly suggested that the domestic environment was the cause of HP. Demonstration of precipitating antibodies to A fumigatus, as well as the dose-dependent inhibition of the IgG to this mold with an
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